practical Flashcards
cerebral congestion(enghephalitis)
Definition:
Congestion is the hyperemia which occurs through an arterial, active mechanism.
Morphology
Macroscopically:the aspect of the organ is:
larger
heavier
blood-red
warmer
pulsatile
painful
Microscopically:
enlarged capillaries, filled with blood
Evolution:
The pattern may return to normal when the causative factors dissapear
Complications that may occur: edema and micro-hemorrhages
Subdural hematoma
A hematoma is a well delineated collection of blood, which appears in different organs (e.g. frequently in the brain, skeletal muscle, but also in other organs)
Macroscopy of hematoma:
nodular or oval, pushing the normal tissue
With a slow change in color (gradually, from red to purple, then green and yellow, following the normal bilirubin breakdown) until its disappearance
Microscopy of hematoma:
erythrocytes extravasate into the interstitium and release hemoglobin. Under the action of inflammatory proteases, hemoglobin is gradually transformed into hemosiderin (brown color), then incorporated in macrophages (siderophages), which together with the lymph remove the hematoma
Evolution of hematoma:
Complete resorbtion, in the case of small hematomas
Enclosure, in the case of large hematomas. They cannot be totally resorbed, but may be slowly surrounded and encased in connective tissue. A yellowish serous component remains usually in the center and hemosiderin and calcium may finally precipitate in the connective tissue which surrounds the old hematomas
Infection of the hematoma, if an infection develops in the proximity of the hematoma
Fibrosis of the entire hematoma – resulting in a small scar which, in some cases it may involve depositions of hemosiderin and calcium
Hemopericardium and cardiac tamponade
Hemopericardium refers to blood in the pericardial sac of the heart. It is clinically similar to a pericardial effusion, and, depending on the volume and rapidity with which it develops, may cause cardiac tamponade.
compression of the heart by an accumulation of fluid in the pericardial sac.
Pulmonary artery thromboembolism
embolism is the mobilization and migration through the bloodstream of a structure named embolus, structure other than blood or aqueous solutions\ hydrosoluble fluids
pulmonary thrombembolism is still a frequent cause of death
old arterial thrombus
What is THROMBOSIS?
Definition:
Thrombosis is the coagulation of blood inside blood vessels and the heart in a living organism.
Predisposing factors for the formation of thrombus (the Virchow triad)
Quallity of the vessel vall (endothelial lesions)
Nature of the blood flow (disorders of the circulation like stasis or turbulent flow)
Composition of the blood (factors causing hyper coagulation)
- The lesions of the vascular wall may have a crucial role in the thrombus formation, and may particularly appear in the following circumstances:
in the arteries: atherosclerosis, HT, artheritis, action of chemical factors (nicotine)
in the veins: sclerosing substances, hypoxia, neoplastic invasion
in the capillaries: extreme temperatures (cold, warm)
- Disorder of the circulation:
a. Stasis (decrease in the speed of the bloodstream)
appears in:
heart failure, bed-ridden patients, phenomena of local stasis
effects:
the contact between thrombocytes and endothelial cells, the local accumulation of activated factors of coagulation produced by endothelial cells (which are normally washed by the rapid bloodstream), and the hypoxia of the stasis affects the endothelial cells.
b. The turbulent flow makes the blood elements to impact against the vascular wall which may cause endothelial lesions:
aneurysms, hidrostatic varices
at the site of vessel branching
preexisting lesions that traumatize the vascular wall (atheroma, mural thrombi)
vegetations or valvular verucae
- The hypercoagulation of blood can occur in:
some genetic diseases or
under the action of some factors acquired during lifetime.
Macroscopy of thrombus:
A. Differences between thrombus and postmortem clot:
The thrombus is:
adherent
frail
undeformable
dull
The clot is:
non-adherent
elastic
deformable
glossy
Evolution of thrombus:
- Autolysis (of small thrombi)
the activation of fibrinolysis
- The organization in connective tissue (of larger thrombi): thrombus->granulation tissue->connective tissue scar
- PMN penetrate into the thrombus and slowly remove the fibrin using hidrolytic enzymes
- macrophages engulf the remaining fibrin and blood cells
- myofibroblasts enter from the base of the thrombus and multiply inside the thrombus
- from vasa vasorum, the endothelial cells multiply and enter the thrombus forming small capillaries, initially without basement membrane (it is formed later)
- the mixture of myofibroblasts, macrophages, neutrophils, other inflammatory cells and the numerous new formed capillaries, form the granulation tissue- the first step in connective tissue scarring
- myofibroblasts produce collagen fibers that have contractile properties (the contraction of the thrombus)
- the capillaries lose their lumen and slowly disappear
- finally, the thrombus transforms in a connective tissue scar
advantage: it fixes the thrombus to the wall (prevent thrombembolism)
disadvantage: stays attached permanently, like a mass that deforms and obstructs the vessel - The recanalization of the thrombus (partial reestablishment of the blood flow):
partial lysis of the thrombus
contraction of the myofibroblasts generates a space between the thrombus and the vascular wall
the newly formed capillaries in the thrombus (angiogenesis) grow along the vascular axis, crossing the thrombus
- The noninfectious (sterile) degradation of the thrombus:
In large thrombi, that have a small connection with the walls of the veins, neutrophils enter and, with the help of their enzymes, melt the thrombus, liquefying its central core
- The infective degeneration of the thrombus:
Is encountered in thrombi colonized by bacteria, derived from an infectious source
Infected thrombi can generate emboli, further spreading the infection
- The calcification of the thrombus:
calcium deposits may form inside venous thrombi (phlebolites) or on endocardial vegetations
- The mobilization of thrombus:
By partial desintergation of the thrombus and its dislodging, the fragments may enter the bloodstream
cerebral Purpura
internal hemorrhage
the exit of blood outside the blood vessels in a living organism
rupture
erosion
erythrodiapedesis
acute pulmonary edema
What is EDEMA?
Definition:
the increase of fluids in the interstitial compartment
Pathogenesis:
Increase of hydrostatic pressure: hyperemia
Decrease of the oncotic pressure: hypoproteinemia
The retention of Na ions
Disorders of lymphatic circulation: lymphedema
Glotic edema:
Definition:
the accumulation of liquid in the glotic mucosa
Etiopathology:
- acute respiratory infections
- immune reactions: angioedema (the Quincke edema)
Evolution:
death caused by asphixiation (suffocation) unless an emergency tracheostomy is performed
cachexia
Atrophy by malnutrition
occurs when the tissues and cells do not receive their basic energetic needs, in other words their normal nutritional requirements
Examples:
the lack of minimal nutritional intake (food deprivation)
the lack of nutrient absorption (GIT diseases)
loss of nutritional substances (vomit, diarrhea, etc.)
Terminology used in case of atrophy by malnutrition:
Tissue-wasting
Cachexia: extreme weight loss in adult
Athrepsia (or athrepsy): extreme weight loss in infants
Left ventricular hypertrophia
Left ventricular hypertrophy is enlargement and thickening (hypertrophy) of the walls of your heart’s main pumping chamber (left ventricle). Left ventricular hypertrophy can develop in response to some factor — such as high blood pressure or a heart condition — that causes the left ventricle to work harder.
hypertrophy is the increase in size and function of an organ which implies the increase in size and function of each constituent cell
The cells become bigger, with a larger nucleus and with more structural components (mitochondria, endoplasmic reticulum etc.)
Hypertrophy appears in permanent cells, particularly in muscle cells, but it can also appear in stable cells.
Nodular hyperplasia of the prostate urinary bladder hypertrophia
Benign prostatic hyperplasia (BPH) is an enlarged prostate gland . The prostate gland surrounds the urethra, the tube that carries urine from the bladder out of the body. As the prostate gets bigger, it may squeeze or partly block the urethra. This often causes problems with urinating
hyperplasia is the increase in size and function of an organ by the increase of the number of its constituent cells
Affects the labile cells, but can also appear in stable cells.
It may appeear simultaneously with hypertrophy
Hyperplasia and hypertrophy should be differentiated from hypergenesis, which involves the congenital overdevelopment of an organ
Gangrene
The gangrene
gangrene is a particular type of necrosis and subsequent degradation of a tissue through an ischemic mechanism sometimes associated with a superposed bacterial infection. Most frequently it occurs at the limbs and in some internal organs.
Dry gangrene:
Definition: coagulative necrosis through an ischemic mechanism of tissues exposed directly to the air.
Bedsores
are localized injuries to the skin and/or underlying tissue that usually occur over a bony prominence as a result of pressure, or pressure in combination with shear and/or friction. The most common sites are the skin overlying the sacrum, coccyx, heels or the hips, but other sites such as the elbows, knees, ankles or the back of the cranium can be affected.
Bronchial squamus metaplasia
metaplasia is the replacement of a tissue with another type of tissue.
The metaplastic tissue is histologically normal, but its location is abnormal.
The young cells of a tissue proliferate and also change their type of differentiation
It does not occur in adult, mature or “differentiated” cells
n the bronchi (airways): the ciliated columnar pseudo-stratified epithelium is replaced with squamous epithelium. This process can be triggered by smoking, chronic bronchitis etc. The new type of epithelium has greater resistance to the aggressive agents, but it is the first step which makes possible the development of bronchial squamous carcinoma
n the bronchi (airways): the ciliated columnar pseudo-stratified epithelium is replaced with squamous epithelium. This process can be triggered by smoking, chronic bronchitis etc. The new type of epithelium has greater resistance to the aggressive agents, but it is the first step which makes possible the development of bronchial squamous carcinoma
Gall stone cholesterol
lithiasis is the appearance of calculi in various areas of the body
Calculi are precipitate phases in a solution situated in an excretory tract
Pathogenesis:
the increase of crystalloids in a secretion (eg : salts in the urine, bilirubin in the bile)
the presence of a precipitation nucleus (i.e.: desquamated cells, microbes, foreign organisms)
Stasis of secretion which favors the infection of the increased amount of secretion
Serus pleurisy
Inflammation of the pleura, usually occurring as a complication of a disease such as pneumonia, accompanied byaccumulation of fluid in the pleural cavity, chills, fever, and painful breathing and coughing.
vesicle(bulla)
vesicle (liquid deposit, less than 1 cm diameter)
bulla (liquid deposit, more than 1 cm diameter
Inflammations of the pavimentous epithelium: serous